| MERCY HOSPITAL | MAGEE HOSPITAL | ||||||||
|---|---|---|---|---|---|---|---|---|---|
| Leucocyte Count. | Influ. | Influ. Pn. | Influ. Compl. | Total | % | Influ. Influ. Pn. Influ. Compl. | % | Total | % |
| 2000 or less | 2 | 2 | 38 | 1 | 28 | 3 | 32 | ||
| 2000–3000 | 3 | 3 | 1 | 7 | 13 | 20 | |||
| 3000–4000 | 7 | 12 | 4 | 23 | 34 | 57 | |||
| 4000–5000 | 14 | 13 | 9 | 36 | 41 | 77 | |||
| 5000–6000 | 17 | 16 | 6 | 39 | 42 | 81 | |||
| 6000–7000 | 15 | 13 | 6 | 34 | 40 | 59 | 37 | 93 | 38 |
| 7000–8000 | 7 | 8 | 5 | 20 | 36 | 56 | |||
| 8000–9000 | 8 | 14 | 8 | 30 | 37 | 67 | |||
| 9000–10000 | 15 | 9 | 8 | 32 | 39 | 71 | |||
| 10000–12000 | 4 | 12 | 9 | 25 | 20 | 44 | 27 | 69 | 25 |
| 12000–14000 | 1 | 1 | 8 | 10 | 28 | 38 | |||
| 14000–16000 | 5 | 3 | 2 | 10 | 22 | 33 | |||
| 16000–18000 | 3 | 2 | 2 | 7 | 16 | 23 | |||
| 18000–20000 | 2 | 2 | 2 | 6 | 15 | 21 | |||
| 20000–22000 | 1 | 1 | 2 | 2 | 4 | 5 | 6 | 3 | |
| 22000–24000 | 1 | 1 | 8 | 9 | |||||
| 24000–26000 | 1 | 1 | 4 | 5 | |||||
| 26000–28000 | 2 | 2 | |||||||
| 28000–30000 | 1 | 1 | 3 | 4 | |||||
| 30000–32000 | 3 | 3 | 3 | 2 | |||||
| 32000–34000 | 3 | 3 | |||||||
| 34000–36000 | 3 | 3 | |||||||
| 36000–38000 | |||||||||
| 38000–40000 | 1 | 1 | |||||||
| 40000–42000 | 2 | 2 | |||||||
| 287 | 460 | 747 | |||||||
The blood picture in uncomplicated influenza is a normal one for the red cells and the hæmoglobin, but the white cells are characteristically altered. We have made many observations on the red blood cells, and from all aspects the picture appears to be normal. Similarly, there is nothing significant about the hæmoglobin estimations. Where we have slight alteration in the red count and in the hæmoglobin it is probably safer not to attribute the change to the epidemic. We have no records showing a secondary anæmia due to the initial epistaxis.
A leucopenia or a normal count is what one should see in most of the uncomplicated influenzal cases. We are almost ready to say that any estimation above normal limits means secondary bacterial invasion. The count may remain low throughout the illness, rising to the normal rapidly as the temperature falls. We do not regard a leucocytosis at the end of an epidemic case as part of the blood picture. Our experience is that with convalescence the normal count returns and remains within normal bounds. Very often hidden sinus infection is responsible for some of the post-influenzal leucocytoses. The leucopenia may vary from a slightly subnormal count to a point well below 2,000. Most of the simple epidemic cases showed some degree of leucopenia. As far as we have been able to estimate, we are led to believe that one should not lay any special stress on the grade of leucopenia as being of prognostic significance in uncomplicated influenza. Many of the mildest clinical types showed very low counts, and vice versa. There is, however, a prognostic relation to be noted with reference to a falling white count in the pneumonia, but this we shall mention again later. The onset of the leucopenia corresponds to the onset of the disease. It was present with the earliest cases we examined, and remained fairly stationary, although we have records of its fluctuating slightly one way or the other. But one must remember in this regard the personal error in blood counting, and also particularly the error of the apparatus. For careful work only those counting chambers and pipettes should be used that have a Bureau of Standards certificate. The duration of the leucopenia was fairly close to the duration of the disease.
How many cases of influenza of several days’ illness having about 12,000 leucocytes, a few sticky râles in the chest, but no signs of definite consolidation, have been observed by the clinicians? These cases recover without further change, and the diagnosis is handed in as influenza without a complication being mentioned. In collecting the blood reports from this group the 12,000 cells accordingly must be considered as having occurred in a simple influenza. We hold that this is not a case of uncomplicated epidemic disease. There is undoubted evidence, as is acknowledged by the clinician, of a bronchiolitis; and how many lungs showing a bronchiolitis at autopsy fail to have a broncho-pneumonia? True it may not be demonstrable by our physical examination. This is often the origin of many high counts in what apparently is considered uncomplicated influenza.
The blood picture of the pneumonia following the epidemic was more or less constant, although at the same time the features of the count may be quite different. One could roughly divide the results into three groups: (1) leucocytosis, (2) leucopenia, (3) intermediate or normal. Some pneumonias could be followed during their course through all of these classes. Before discussing the white count we can briefly dismiss the other phases of the blood examination by stating that the red blood cells and hæmoglobin presented nothing by the usual examinations which was of special significance, or in any way characteristic.
As an example of the group showing a leucocytosis let us follow a patient through an acute influenzal attack, followed by a pneumonia with a subsequent recovery. An initial leucopenia, gradually or suddenly changing into a very moderate leucocytosis (10,000–15,000), was noted at the onset of the pneumonia. During the course of the complication the number of cells in the majority of cases increased, but rarely advanced beyond 20,000. With lysis or crisis the count dropped toward normal, and by the time the lung signs had disappeared the white cells were at the usual number, or very slightly increased. The point which seemed to us to be of importance was that, even although we had a leucocytosis, it was nothing like the count that one would expect for a lobar pneumonia. Of course, there were a few high counts, but looking at the group as a whole they were relatively low. There are a number of variations to this form of blood picture which we might briefly consider. We have observed secondary rises in the leucocyte count concurrent with a new lung involvement. This type was the one so prone to develop into a condition of non-resolution, fibrosis and ultimate death, with a continuous moderately high leucocytosis to the end. Another variation which we learned to fear was the fall of leucocytes to normal or subnormal after a primary rise, when the clinical course of the case in no way indicated a crisis or lysis pending. Seemingly, the longer the primary leucocytosis had been present the more serious was the subsequent leucopenia. We regard this form of secondary leucopenia, if one may use such a term, as a prognostic sign of some value. As in lobar pneumonia, a high leucocyte count has been, as a rule, a favorable feature.
The second group, or those showing a leucopenia throughout their course, was by no means an unusual thing. This is a cardinal point—in fact, one of the most striking clinical features of the epidemic. The leucopenia here does not have the prognostic value that it seems to have in the group just referred to previously. We have observed cases go through a pneumonia with 4,000–5,000 white cells in a relatively easy manner. When, however, the leucocytes fall to 3,000 or under, one may be reasonably sure that the outcome is doubtful, even with the general condition of the patient at the time favorable. In the pneumonias of this group which died the leucocytes have always fallen to about 2,000 cells. We have a number of observations taken from one-half to four hours before death showing counts in the immediate neighborhood of 2,000, but never below this number. Where recovery has taken place the cells go forward to the normal, more or less keeping pace with the general clinical picture.
Of group three there is not much to say, except that on one hand it tends toward a leucocytosis, and on the other to a leucopenia. This group comprises a considerable number of the pneumonias. We are not in a position to say anything regarding the relative mortality of this group. The development of a leucopenia from these cases after a period of some stability in the leucocytic curve is of bad prognostic import. Not infrequently we have noticed rather wild abrupt rises to 20,000 in the leucocytes toward the late half of the disease. This curve was nearly always sustained until the end, which, as a rule, was recovery.
We do not need to consider at any length the effect on the leucocyte count of complications not of lung origin. Acute sinuses in head, otitis media and meningitis always produced a variable moderate leucocytosis. The change was not so marked in meningitis, as our cases were all preceded by a pneumonia which had independently invoked a slight leucocytic response. As a complication of the pneumonia we have noted an abrupt rise following an acute pleuritis with effusion, and similarly after the onset of an empyema. These complications seemed to be able to induce a leucocytosis with more certainty and ease than the more serious pneumonic condition. Possibly, as they occurred toward the end of the infection, the toxic factor of the epidemic influenza was more or less spent, and the secondary invader had a freer hand to act in its normal way.
Differential counts were made in 194 cases, including influenza, influenzal pneumonia and influenzal complications. We have taken the average percentage of each type of cell for the groups, which are purely numerical divisions based on the leucocytic count. No differentiation is made for the various clinical divisions of the epidemic in the following table: